Crohnʼs Disease in HIV-infected Children: A Report of 2 Cases

Abstract

Inflammatory bowel disease is infrequently reported among HIV-infected adults and rarely in children. The course of IBD may be less severe in HIV-infected patients because of underlying immunosuppression from the virus. One perinatally HIV-infected adolescent and one HIV-infected young adult were diagnosed with Crohn's disease at the University of Miami Pediatric Gastroenterology Program. A retrospective review of medical records including history, physical examination, laboratory, radiographic and pathology results was performed. Case 1: A 20 year-old African American male acquired HIV early in infancy, presumed secondary to pre mastication of food. A life-long history of noncompliance with antiretroviral medications improved recently with increased CD4 count by over 300% (42 to 144 cell/mm3) and viral load from 1,452 to 838 copies/mL one month prior to presentation. He presented with abdominal pain, intermittent bloody diarrhea, nausea, and weight loss over 6 months. He had history of aphthous oral ulcers and right knee pain. Skin tags were noted on rectal exam. EGD revealed nodularity in the stomach. Colonoscopy showed aphthous ulcers scattered throughout the colon with friable intervening mucosa. Histopathologic examination of biopsies showed Helicobacter pylori-associated chronic active gastritis and villous blunting of the duodenum with chronic inflammation of lamina propria. Colonic biopsies revealed acute inflammation of lamina propria with occasional eosinophils and intervening normal tissue. Special tests for infectious pathogens were negative. IBD antibody panel revealed positive C-ANCA. UGI/ SBFT was normal. H. pylori was managed with triple therapy. High dose steroids and mesalamine were started. Case 2: A 13 year-old African American boy with vertically-acquired HIV was chronically under control with CD4 counts >35% and viral loads <200 copies/mL. History of chronic failure to thrive led to gastrostomy tube placement for nutritional supplementation in infancy. He developed acute pancreatitis at the age of 10 years, endoscopy revealed focal acute duodenitis. Abdominal CT revealed bowel wall thickening of several loops. He was lost to GI follow-up for 3 years after which time he presented with early satiety, nausea, poor weight gain, and oral ulcers. There was diffuse abdominal tenderness. Laboratory work up revealed a positive ASCA IgA (117.5 u, normal ≥ 20 u). MR-enterography was normal. Repeat EGD revealed focal chronic esophagitis and focally eroded fundic mucosa. Colonic biopsies revealed patchy active colitis with cryptitis, supporting the diagnosis of Crohn's disease. High-dose corticosteroids were initiated with improvement in appetite and oral ulcers. Thiopurines and mesalamine were started with a corticosteroid taper. Two months later, remarkable weight gain with improved appetite and tolerance to gastrostomy supplementation was noted. We describe 2 cases of HIV diagnosed in infancy presenting with Crohn's disease at the time of improved immunocompetence secondary to immunoreconstitution in one, and as a lifelong HIV non-progressor in the second. Our pediatric cases suggest that intact immunity plays a role in the expression of IBD in this population. As HIV-infected children have an increased life expectancy due to effective therapies, early suspicion for IBD in individuals with suggestive symptoms is warranted. Close monitoring for opportunistic infections and emergence of malignancies with treatment is essential.